Abdominal Flashcards

Question

How is bilirubin produced?

Answer 1

``` #Bilirubin is the end product of haem metabolism 80% of bilirubin is produced from the breakdown from haemobglobin in RBCs and 20% from the breakdown of haem in myoglobin and cytochromes. ```

Answer 2

The causes can be classified as Pre-hepatic , hepatic and post-hepatic causes. Prehepatic: when bilirubin production is increased through exercise, haemoglobin breakdown (haemolysis) or myoglobin breakdown (rhabdomyolisis). Haemolysis can be intrinsic where the RBC is defective or extrinsic, where RBC is normal. Hepatic: bilirubin increases in any process in which cell necrosis reduces liver’s ability to metabolize and excrete bilirubin such as: Acute hepatitis and liver cirrhosis of any cause, enzymopathies such as Gilbert’s syndrome and Crigler-Najjar syndrome. Posthepatic: when there is an obstruction of biliary drainage system causing their reflux to blood. Within the liver: PBC, PSC, drugs. Extrahepatically: gallstones, pancreatic Ca, parasites.

Answer 3

FBC, LFTs, hepatoglobulins, reticulocytes, coom’s test, clotting profile, autoimmune screen, viral screen. Urine test. Further: USS abdo, CT abdo, ERCP, MRCP, liver biopsy

Answer 4

Autosomal dominant condition resulting in reduced levels of the enzyme glucuronyltransferase. This results in reduced conjugation of bilirubin.→ lvls of unconjugated bilirubin ↑. Precipitated by stress, fasting, infection. Condition is benign and asymptomatic, no treatment necessary.##What is Dubin-Johnson syndrome? Autosomal recessive defect in molecular transporters responsible for excreting conjugated bilirubin out of hepatic cells. → ↑levels of conjugated bilirubin and pigmentation of the liver

Answer 5

Findings: Jaundice Hands: clubbing, leuconychia, hyperpigmentation, excortiation, purpura, xantomata, dupytren;s contracture, palmar erythema, hepatic flap Trunk: hepato-, spelno-megaly, ascites, caput medusa, spider naevi, gynaecomastia Other: scanty body hair, testicular atrophy, ankle oedema, tattoos, needle marks →? IVDU

Answer 6

It’s a consequence of chronic liver disease. Characterised by a replacement of normal liver tissue by fibrous scar tissue and regenerative nodules, which leads to a loss of liver function.

Answer 7

``` Ascites Spontaneous bacterial peritonitis Coagulopathy Portal HTN Hepatic encephalopathy Hepatorenal syndrome HCC ```

Answer 8

``` Infection Drugs: diuretics and sedatives Upper GI bleed Abdo paracentesis Surgery ```

Answer 9

More common in females. Associated with autoimmune conditions such as type 1 diabetes, thyroiditis, RA, scleroderma, IBD. Presents with fatigue, RUQ pain, arthralgia, abnormal LFTs Tx with immunosuppressive drugs (steroids, azathioprine) 80% are associated with HLA B8/DRw£, ANA, anti-smooth muscle antibodies and polyclonal hypergammaglobulinaemia.

Answer 10

Defective production of alpha-1-antitrypsin, which is a protease inhibitor. There are several forms and degrees of deficiency. Deficiency results in cirrhosis, increased risk of HCC, emphysema. Tx by liver and lung transplantation.

Answer 11

It is a DNA virus Transmitted perenterally or by sexual contact. Complications include liver cirrhosis and HCC. Tx with interferon-alpha is successful in about 40% of cases. SEs include flu-like sx, depression, fatigue, haematological abnormalities. Other drugs: lamivudine, adefovir, entecavir.

Answer 12

It is an RNA virus. Main routes of transmission: through needles in IVDU, blood transfusions, blood products. Sexual transmission is low. Complicaitons: liver cirrhosis, HCC. Tx: interferon-alpha and ribavarin.

Answer 13

Emphysema – overinflated lungs# Reidel’s lobe R-sided pleural effusion

Answer 14

Characterised by thrombosis of the hepatic veins, resulting in: abdo pain, ascites, hepatomegaly Jaundice usually absent No cutaneus features of liver disease as the onset of liver failure is rapid Liver is smoothly enlarged and tender

Answer 15

Hypercoagulabloe states: pregnancy, contraceptive pill, PRV, essential thrombocythaemia, antiphospholipid syndrome, Protein C, S or antithrombin III deficiency HCC Hepatic infections such as hydatid disease Renal and adrenal tumours Congenital venous webs

Answer 16

I would like to complete my examination by CHECKING FOR LYMPHADENOPATHY IN THE AXILLAE, CERVICAL AND INGUINAL AREAS.